Actual position:Directeur d'Unité UMR-S 1180: "Signaling and Cardiovascular PAthophysiology"
2011-2015: "Directeur de Recherche" INSERM. Head of Inserm team: "Calcium Signaling and Cardiac physiopathology", at U-769 Inserm Unit
1991-1994: Ph.D. at Instituto de Farmacología y Toxicología, CSIC-Universidad Complutense de Madrid, Spain, on "Heterogeneity of ionic currents in the normal and hypertrophied rat cardiac ventricle".
1995-1997: Post-doctoral stage at Univesrity of Maryland Biotechnology Institute at Baltimore, USA. Research on "Calcium sparks in normal and hypertrophied hearts".
1998-2008: Tenure position as Chargée de Recherche at CNRS.
From 2008: Tenure position as Directeur de Recherche at INSERM.
Cardiovascular diseases remain the leading cause of death in developed countries. Last stage of cardiac pathologies, heart failure is major cause of morbidity and mortality. Despite therapeutic improve, HF patient’s prognostic is very poor, and more than 50% dye suddenly as consequence of ventricular arrhythmia. This fact is the consequence of misunderstanding of the molecular mechanisms responsible of contractile dysfunction and arrhythmogenesis. It is thus imperative to elucidate the pathological mechanisms in order to find new therapeutic targets and develop efficient pharmacology.
In order to better understand heart failure syndrome, we develop a project program focused in analyzing Ca2+ handling involvement in the genesis of heart failure and arrhythmia. In this sense, in addition of activating cardiac contraction, Ca2+ is recently emerging as a key factor in transcription regulation (excitation-transcription coupling, ETC) and in arrhythmia development. Our project aims to elucidate the adaptive and maladaptive mechanisms involved in cardiac hypertrophy and arrhythmia.
I am expert in cardiac excitation-contraction coupling (ECC) and their alterations in cardiac hypertrophy/heart failure responsible of pump failure and arrhythmia generation. In my first paper we discovered the ionic current involved in the action potential prolongation in cardiac hypertrophy and their heterogeneity within the ventricle (J. Physiol. 1993), what is now well established and generally accepted. Continuing with cardiac hypertrophy, I detected a defect in ECC in heart failure in one of the pioneers papers in Ca2+ sparks (fundamental events in ECC) and the first analysis of Ca2+ sparks in pathology (Science 1997). Since then, I have contributed discovering fundamental signalling pathways involved in heart failure and arrhythmogenesis, publishing in the best specialised journals (5 Circulation , I.F. 14.8; 5 Circulation Research, I.F. 9.2). I have a total of 51 publications that have been cited 2097 times, with 5 articles cited >100 times and an H factor of 22. I am often invited to give conferences in international meetings (25 accepted) and 22 seminars around the world. I have trained a total of 22 persons: 10 undergraduates, 5 Ph.D. students, 7 post-doctoral fellows and 2 sabbaticals.
The biophysical society members (over 8000 worldwide) elected me to become a council member (2006-2009), and I was recently elected Fellow from the European Society of Cardiology.